Lipoprotein lipid transport by livers from normal and CCl4-poisoned animals

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Abstract
Triglyceride release by livers isolated from normal fed animals has been shown previously to be stimulated by the addition of palmitate to the perfusate. It may be concluded from the data reported herein that the output of cholesterol and phospholipid into the d < 1.006 lipoprotein class is proportional to release of triglyceride into this fraction. Triglyceride, cholesterol, and phospholipid may be secreted in constant proportion in order to maintain a physical-chemical stability and solubility of the very low density lipoprotein whose primary function is transport of triglyceride from liver to extrahepatic tissues. CCl4, which inhibits triglyceride release by the liver, also inhibits output of cholesterol and phospholipid into the d < 1.006 lipoprotein. Release of cholesterol into the d < 1.063 lipoprotein is not clearly related to non-esterified fatty acid levels in the medium, to triglyceride release by the liver, or to other lipids present in this fraction. The serum lipoprotein class containing the largest initial concentration of any lipid is not necessarily identical with the fraction having the major net hepatic release of that lipid. Thus, each lipoprotein class released may have specific and different lipid carrier functions.